The present application is in response to Strategy 1.3 of the NIMH strategic plan, which calls for the identification of behavioral indicators of mental disorders that can aid treatment. This goal will be met by delineating divergent patterns of social cognitive ability in Autism Spectrum Disorder (ASD) and Schizophrenia (SCZ) in order to identify disorder specific treatment targets. ASD and SCZ are both characterized by significant social dysfunction, which in adulthood impairs quality of life, impedes independent living and employment, and confers a tremendous economic burden for families and society. Social cognition, a term referring to the skill-set used to interpret social information in real-world contexts, has been proposed as a primary mechanism of this dysfunction in both disorders. Recent promising treatments developed and optimized for adults with SCZ confirm that social cognitive training can improve functional outcome, but attempts to extend these programs to adults with ASD have been far less successful. This discrepancy in treatment efficacy demonstrates that the structure and function of social cognitive impairments in the two disorders are not analogous. The primary hypothesis of the proposed project is that overlapping general deficits in social cognition in ASD and SCZ are supported by unique patterns of impairment across social cognitive domains. By comparing performance on a comprehensive social cognitive battery between 100 adults with ASD and 50 matched controls, and 100 adults with SCZ and 50 controls collected as part of a companion grant (R01MH093432, co-PIs Penn, Pinkham, & Harvey), this proposal aims to specify the profiles of social cognitive deficit in ASD and SCZ (Specific Aim 1), assess the relative contribution of neurocognition to these profiles (Specific Aim 2), and link them to social functioning (Specific Aim 3). It is hypothesized that ASD is characterized by greater impairment than SCZ in basic social perception that serves as the foundation for broader deficits in social appraisal. In contrast, SCZ while exhibiting impairments in social perception relative to healthy controls, will outperform ASD in this area but demonstrate the greatest deficits in social cognitive appraisal. Neurocognition is expected to contribute to social appraisal deficits in SCZ, but be relatively independent of social cognition in ASD. These distinctions are hypothesized to differentially predict social functioning, and thus provide criticl information for future mechanistic and treatment studies addressing social cognitive deficits in both disorders. Further, in contrast to SCZ, the translational relevance of social cognition for adults with ASD has yet to be evaluated, due in part to a lack of well-validated performance based measures of functioning. The current proposal is designed to address this need. Finally, consistent R15 goals, this project will develop the infrastructure for autism research at UT-Dallas and expand training opportunities for undergraduate and graduate students.